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In support of this assumption, it appears that in most patients treated with statins, the skeletal muscle CoQ10 content remains high enough to maintain the ETC function ( Taken together, our data point toward ferroptosis as an essential molecular mechanism leading to statin-induced muscle damage, providing valuable new insights into homeostatic mechanisms required for the tolerance of the widely prescribed atorvastatin

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This release leads to vasodilation, plasma extravasation, leukocyte migration, and an increase in proinflammatory cytokines [208]